Chronic Budd-Chiari Syndrome Research Articles

Chronic Budd-Chiari syndrome as an initial manifestation of primary antiphospholipid syndrome in a young patient.

Chronic Budd-Chiari syndrome as an initial manifestation of primary antiphospholipid syndrome in a young patient.

Aetiology and diagnostic utility of serum ascites albumin gradient in children with ascites

BackgroundAscites in children is multifactorial and serum ascites albumin gradient (SAAG) ≥1.1 helps differentiate portal hypertension (PHTN) related from non-PHTN ascites. AimsWe evaluated the aetiology and diagnostic accuracy of SAAG in children with ascites. MethodsChildren with ascites were retrospectively evaluated. Etiological diagnosis was based on clinical presentation and investigations. All cases with ascitic fluid analysis and a definite diagnosis were included for calculating the utility of SAAG. ResultsWe enrolled 878 children (568[64.7%] boys). Majority were PHTN related (638[72.7%]) and secondary to acute viral hepatitis (98,15.4%), acute liver failure (185,29%), chronic liver disease (276,43.3%) and Budd-Chiari syndrome (79,12.4%). Other causes included tubercular (46,5.2%), pancreatic (32,3.6%), chylous (20,2.3%), biliary (12,1.4%), pseudoascites (16,1.8%), infections (46,5.2%), nephrotic (26,2.9%), malignancy (23,2.6%), cardiac (9,1.0%) and others (10,1%). SAAG (n = 305) correctly differentiated PHTN and non-PHTN ascites in 272 (89.2%) cases, with a high sensitivity (97%), specificity (93%) and diagnostic accuracy (95.8%). Reasons for inaccurate SAAG included mixed ascites (n = 9), different day serum and ascitic fluid albumin estimation (n = 5), serum albumin ≤1.1 g/dL (n = 2), chylous ascites (n = 3), hypergammaglobulinemia (n = 1), albumin infusions (n = 1) and unexplained (n = 12). ConclusionsNearly 27% children had non-PHTN related ascites. SAAG differentiates PHTN from non-PHTN ascites with a diagnostic accuracy of 95%.

S3493 Large Microcystic Appearance of Centilobular Venous Congestion in a Case of Acute on Chronic Budd-Chiari Syndrome

S3493 Large Microcystic Appearance of Centilobular Venous Congestion in a Case of Acute on Chronic Budd-Chiari Syndrome

Budd-Chiari Syndrome Imaging Diagnosis: State of the Art and Future Perspectives.

Budd-Chiari syndrome (BCS) is a rare hepatic vascular disorder defined by the presence of partial or complete impairment of hepatic venous drainage in the absence of right heart failure or constrictive pericarditis. Several conditions can lead to BCS, from hypercoagulable states to malignancies. Primary BCS is the most common subtype, and usually bartends hypercoagulability states, while secondary BCS involves tumor invasion or extrinsic compression. A combination of clinical and imaging features leads to the diagnosis of BCS, including (1) direct signs: occlusion or compression of the hepatic veins and/or inferior vena cava, and the presence of venous collaterals; (2) indirect signs: morphological hepatic changes with caudate lobe enlargement; inhomogeneous enhancement, and hypervascular nodules. From a clinicopathological point of view, two forms of BCS can be distinguished: acute and subacute/chronic BCS, although asymptomatic and fulminant forms are also possible. Acute presentations are rare, and symptoms include hepatomegaly, ascites, and hepatic insufficiency. Subacute/chronic forms are the most common presentation, with dysmorphic liver and variable degrees of fibrosis deposition. Patients with chronic BCS can develop benign regenerative nodules (large regenerative nodules or FNH [Focal Nodular Hyperplasia]-like lesions), but are also at a higher risk of hepatocellular carcinoma (HCC). The radiologist role is therefore fundamental in both diagnosis and surveillance of BCS. The aim of this review is to present all clinical and imaging signs that can help to reach the diagnosis of BCS, with their clinical significance, providing tips and tricks for the cross-sectional diagnosis of this condition.

Multiple hemangiomas (hepatic small vessel neoplasia) in the liver with Budd-Chiari syndrome.

Hepatic small vessel neoplasia (HSVN) is a recently recognized hemangioma of the liver with uncertain malignant potential. Almost all the patients are asymptomatic. Budd-Chiari syndrome (BCS) is a rare disorder characterized by noncardiogenic hepatic venous outflow obstruction. Benign hepatocellular nodules have been acknowledged for a long time in the liver with the chronic BCS. However, there has been no case report of BCS associated with HSVN. The patient was diagnosed with BCS 13years ago. The imaging test initially displayed multiple hepatic nodules that were suspected of benign hepatocellular nodules. They gradually increased in size and number in the course of the disease. At an autopsy, these nodules were confirmed to be multifocal HSVN. The tumor of the present case could not be proved to have GNAQ and GNQ14 mutations. We describe the case focusing on the chronological imaging changes and discuss on the relationship between BCS and HSVN.

Prevalence of Portal Vein Thrombosis in Budd-Chiari Syndrome Patients

Background and Aim: Thrombosis of the portal vein or obstruction of the hepatic venous outflow tract is the cause of portal vein thrombosis (PVT) and Budd-Chiari syndrome (BCS). Patients with PVT may experience a shorter survival rate compared to those without. The present study aimed to determine the portal vein thrombosis occurrence in Budd-Chiari syndrome patients. Patients and Methods: This cross-sectional study was conducted on 46 Budd-Chiari syndrome patients in Gastroenterology department of DHQ Teaching Hospital and Mufti Mahmood Memorial Hospital, Dera Ismail Khan from November 2021 to October 2022. Written informed consent was taken from each individual. Doppler ultrasonography (colored-pulsed) was used to confirm the PVT and BCS cases. Clinical data, laboratory findings, and radiological data were recorded. SPSS version 26 was used for data analysis. Results: The overall mean age of the BCS patients was 28.34±4.6 years. The prevalence of portal vein thrombosis in BCS patients was 12.8% (n=6). Of the total cases, the incidence of chronic and acute BCS presentation was 42 (91.3%) and 4 (8.7%) respectively. The most prevalent symptoms of BCS were abdominal pain and abdominal enlargement in 38 (82.6%) and 41 (89.1%) respectively. Hepatomegaly and ascites were most prevalent clinical signs found in 36 (78.3%) and 37 (80.4%) respectively. The incidence of esophageal varices, gastric extension, and fundal varices were 32 (69.6%), 4 (8.7%), and 2 (4.3%) respectively. About 21 (45.7%) cases had Portal hypertensive gastropathy (PHG). Conclusion: A higher incidence of PVT was observed in the present study than previously reported. Sociodemographic data and underlying etiology of BCS were not significantly different between patients with and without PVT. Those with PVT were more likely to experience hepatic tenderness, increased white blood cells, and increased direct bilirubin. PVT and other patients had similar Doppler ultrasound findings. Keywords: Portal vein thrombosis, Prevalence, Budd-Chiari syndrome

Severe polycystic liver disease: An unsual cause of chronic Budd-Chiari Syndrome

Autosomal dominant polycystic kidney disease is a hereditary disease, characterized by the development of cysts in the renal parenchyma with extra-renal manifestations. Liver damage is rarely a source of complications. A Budd-Chiari syndrome could occur following the compression of the supra-hepatic veins by the cysts. It is an exceptional mechanical complication. We present a case of a 54 year old woman, with a diagnostic of an asymptomatic autosomal dominat polycystic kidney disease since childhood was admitted to our hospital due to significantly increased abdominal girth. The physical examination showed grade III ascites. A paracentesis for relief at admission disclosed an exudative fluid. A abdominal computed tomographic scan showed multiples cystic lesions in the kidneys and liver, with a large hepatic cyst responsible for compression of the suprahepatic veins and the inferior vena cava resulting in chronic Budd-Chiari syndrome. The treatment was radiological drainage followed by percutaneous sclerosis of cysts to alleviation of the compression. Unfortunately, the patient died a few days after an intraperitoneal cystic rupture.

Occurrence of Chronic Budd-Chiari Syndrome in a Patient with Coeliac Disease

The association of Budd-Chiari Syndrome (BCS) with coeliac disease has been understudied and underreported. Majority of the cases of this association have been reported from North Africa and Southern Europe, due to a higher prevalence of coeliac disease. BCS can present as acute, subacute, or chronic form and is characterised by hepatic venous obstruction, either thrombotic or non-thrombotic without any evidence of sinusoidal obstruction syndrome, right heart failure or constrictive pericarditis. Unlike patients with BCS alone, an underlying hypercoagulable state cannot be identified in most patients if coeliac disease is associated with BCS. Its incidence is found to be low in the rest of the world. Here, we present a case of coeliac disease and BCS from an Indian setting in a patient who was previously diagnosed with coeliac disease six years back, maintained on a gluten-free diet, and now presented with complaints of chronic Budd-Chiari Syndrome without any identifiable hypercoagulable aetiology.

Percutaneous Sclerotherapy for Budd-Chiari Syndrome Secondary to Giant Hepatic Venous Malformations (Hemangiomas)

This prospective study evaluated the safety and effectiveness of percutaneous sclerotherapy in the treatment of secondary Budd-Chiari syndrome due to hepatic venous malformations (HVMs). Four patients (mean age, 40 years; 3 women) with 5 HVMs underwent 7 sessions of percutaneous sclerotherapy with a mixture of bleomycin and lipiodol. All patients had chronic Budd-Chiari syndrome, determined based on imaging findings, with the main symptom being abdominal discomfort and distention. On physical examination, 2 patients had ascites and the other 2 had an epigastric mass. The indication for treatment was intractable abdominal symptoms due to hepatic and/or inferior vena cava (IVC) outflow compression. All procedures were technically successful, with no major complications. Three patients underwent a second session because of incomplete IVC decompression. The patients’ symptoms completely resolved at 6 and 12 months of follow-up. There was a significant reduction in lesion volume (P = .007) and an increase in IVC luminal area (P = .018) at 12 months of follow-up.

Combined Transhepatic-Transsplenic Direct Intrahepatic Portocaval Shunt in a Child with Budd-Chiari Syndrome

A 6-year–old girl presented emergently with 3 episodes of hematemesis over 3 days and abdominal distension for 10 days. Physical examination revealed distended superficial abdominal veins. Ultrasonography (US) showed thrombosed hepatic veins and infrahepatic inferior vena cava (IVC) with ascites, which is diagnostic of chronic Budd-Chiari syndrome with portal hypertension. Direct intrahepatic portocaval shunt creation was planned under general anesthesia. Bilateral jugular and brachiocephalic veins were chronically occluded (Fig 1a), and femoral venography showed chronic occlusion of the IVC (Fig 1b).

Utility of Hepatic 2D Shear-Wave Elastography in Monitoring Response to Image-Guided Intervention in Children With Chronic Budd-Chiari Syndrome: A Prospective Study.

BACKGROUND. Image-guided interventions for Budd-Chiari syndrome (BCS) reduce hepatic congestion, thereby reducing liver stiffness. Liver stiffness measurement (LSM) by means of ultrasound may provide a noninvasive marker for assessing treatment response. OBJECTIVE. The purpose of this study was to assess, with attention to changes in LSMs in patients with disease recurrence, the utility of 2D shear-wave elastography (SWE) for monitoring response to image-guided intervention in children with BCS. METHODS. This prospective study included children with chronic BCS and planned image-guided intervention. Color Doppler ultrasound (CDUS) and 2D SWE were performed at baseline; 24 hours, 1 month, and 3 months after intervention; and every 3 months thereafter or when recurrence was clinically suspected. Eighteen children underwent liver biopsy at intervention for fibrosis staging according to the Metavir criteria. Disease recurrence was diagnosed with CDUS. Statistical evaluation was performed by means of nonparametric tests. RESULTS. A total of 32 children (28 boys, four girls; mean age, 9 years; range, 3-14 years) were included. The median LSM at baseline was 43.7 (interquartile range [IQR], 33.0-65.4) kPa, at 24 hours was 22.5 (IQR, 16.8-32.0) kPa, at 1 month was 18.7 (IQR, 14.2-32.0) kPa, and at 3 months was 16.7 (IQR, 11.5-22.5) kPa (p = .001 for all postintervention time points vs baseline). Nine (28.1%) patients had a recurrence at a mean of 4 months after intervention. In one patient with recurrence, LSM was higher at 24 hours (52.3 kPa) than at baseline (44.2 kPa). In the other eight patients with recurrence, LSM was increased at recurrence compared with the prior postintervention LSM (median absolute increase, 11.0 [IQR, 6.1-24.4] kPa). Fibrosis stage was not significantly correlated with baseline LSM (r = 0.11 [95% CI, -0.37 to 0.54]; p = .51) or LSM 24 hours after intervention (r = 0.39 [95% CI, -0.11, 0.73]; p = .11). CONCLUSION. LSMs decreased significantly after image-guided intervention for chronic BCS in children, exhibiting a maximal decrease 24 hours after intervention. Disease recurrence was typically associated with an increase in LSM compared with the patient's prior measurement. CLINICAL IMPACT. LSM obtained with 2D SWE may serve as a useful quantitative adjunct to CDUS in monitoring children with chronic BCS for disease recurrence after percutaneous interventional treatment.

Budd-Chiari Syndrome as an Initial Section Presentation of Antiphospholipid Syndrome in a Male

In Budd-Chiari Syndrome (BCS) there is narrowing and obstruction of the veins of the hepatic veins. Patients have upper quadrant abdominal pain, hepatomegaly and/or ascites. Authors hereby, discuss a case report of a 20-year-old male with history of abdominal pain, progressive distension of abdomen and mild jaundice for two months. He had hepatic vein thrombosis as well as lupus anticoagulant and was positive for anti-beta 2-glycoprotein I antibody indicative of antiphospholipid syndrome. The patient was worked up for hypercoagulable states in view of unusual site of venous thrombus. Patient recovered after being treated with prolonged anticoagulation and hepatic vein stenting. The link between antiphospholipid syndrome and BCS is well documented in the literature, but occurrence of BCS due to primary antiphospholipid syndrome is rare. Early identification, treatment of underlying cause can prevent chronic BCS and liver cirrhosis.

Chronic Budd–Chiari syndrome in paroxysmal nocturnal haemoglobinuria

A 42-year-old woman with a sudden onset of abdominal pain requested to see us urgently. 5 years earlier she had been diagnosed with paroxysmal nocturnal haemoglobinuria (PNH) and had missed multiple follow-up appointments. Despite having a large PNH clone—greater than 50% of PNH granulocytes—the patient had been asymptomatic with only mildly elevated haemolytic parameters and treatment with eculizumab had been deferred.

A Case Report on Budd Chiari Syndrome – Which Mimics Multiple Disorders

Background: Budd Chiari Syndrome (BCS) is the king of disorders which will mimic other disorders like chronic biliary disease, constrictive pericarditis, sinusoidal obstruction syndrome and so on, as it be like that, it is less diagnosed and treated in many countries. The prevalence of BCS is one in one million population, so it is a very rare case therefore it should be treated properly because many disorders like hematologic or malignant disease are the complications of BCS [1], [2].
 Objective: To access the clinical variants of BCS along with the similarities and differences in clinical presentation, diagnostic approaches, and general treatment pattern which mimic, BCS thus gives the physician a clear outline about those disorders.
 Method: A man of 42 years old having BCS was taken for the study to carry out the differences in clinical features of BCS which distinguish the mimicking disorders. Clinical presentations were noted. Laboratory tests and diagnostic tests showed that the patient is having comorbidities including fatty liver with cholelithiasis, mild splenomegaly, liver parenchyma diseases, large esophageal varies with signs of recent hemorrhage, port hypertensive gastropathy and minimal ascites [3]. Patient get discharged after feeling better.
 Result: This patient is having chronic BCS with DIPS dysfunction. The patient had no history of liver disease before diagnosing BCS. BCS is almost curable when it is diagnosed correctly as early as possible. If not diagnosed early and treated well, comorbidities will occur, and it will affect the patient quality of life.
 Discussion: Early detection and proper treatment will help to control the disease up to an extent. This is depending on the physician’s knowledge. Hence, this case study clearly explains the disorders which mimic BCS for better understanding.

Caput medusa: a sign of portal hypertension in case of chronic Budd-Chiari syndrome

<h3>Objectives</h3> We aimed to develop a systematic synthesis of systematic reviews of health impacts of climate change, by synthesising studies’ characteristics, climate impacts, health outcomes and key findings. <h3>Design</h3> We...

Budd-Chiari syndrome computed tomographic imaging: Elucidating the devil in the details.

Hepatic venous outflow obstruction, due to hepatic venous thrombosis is the hallmark of Budd-Chiari Syndrome (BCS), a relatively uncommon disorder. The aim of this study was to explore imaging details and causes, and define invasive and non-invasive interventions for achieving successful portosystemic shunting (PSS). The variations in imaging topology and associated risk factors in BCS cases, diagnosed during the past 20 months, were studied. Of the 53 cases (32 males, 21 females; mean age: 34.4±13.5 years), 5 (9%) were Hepatitis-B virus (HBV) positive, 12 (23%) were HCV positive and 6 (11%) were co-infected, rest were negative. Imaging features included mottled cirrhotic hepatic parenchyma, thrombosed hepatic and portal-vein with or without IVC thrombosis, left lobe atrophy, caudate hypertrophy, splenomegaly, portosystemic varices and ascites. Three cases had subacute onset; two had acute while the rest were chronic BCS. The aetiology was: protein C, S and anti-thrombin deficiency in 24 (45%), JAK2 mutation in 3 (6%), lupus antibody with increased homocysteine levels in 5 (9%) and cryptogenic in 21 (40%) cases. Twelve cases were planned for liver transplantation, 20 were prepared to undergo TIPS, and the rest were optimised medically.

2209 Abdominal Arterial Aneurysms in a Patient With Budd-Chiari Syndrome

INTRODUCTION: Budd-Chiari syndrome (BCS) is defined as hepatic venous outflow tract obstruction. Chronic BCS eventually leads to post-sinusoidal hypertension resulting in the symptoms of the disease. There have been case reports of BCS leading to intra-abdominal bleeding from ectopic varices, however, these are cases of venous bleeding. Here, we report a unique case of a Chinese woman with BCS presenting with bleeding from arterial aneurysms. CASE DESCRIPTION/METHODS: A 61-year-old woman with BCS requiring multiple prior porto-systemic shunting procedures was brought by EMS for coffee ground emesis. At the ED, she was stuporous and developed bloody emesis and hypotension. She was intubated and transferred to the ICU. Exam was remarkable for abdominal distention (AD) with a fluid wave. Labs showed leukocytosis; prolonged coags, elevated troponins, lactate, LDH and decreased fibrinogen and haptoglobin. FAST showed intra-abdominal free fluid. EGD showed grade II varices in the esophagus that were banded. However, the patient continued to deteriorate with increasing AD. CT-AP revealed a cirrhotic liver with occluded left and middle hepatic veins and extravasation of contrast near the greater curvature of the stomach into a LUQ hematoma (Figure 1). IR embolized the left gastric artery and identified aneurysms along a branch of the SMA (Figure 2) in addition to an aneurysm at the celiac artery origin (Figure 3). On the 2nd post-op day, the patient again developed hypotension with AD. Attempted embolization of the SMA branch was unsuccessful. On the 5th post-op day, the family agreed to withdrawal of life support and the patient was extubated and vasopressors were stopped. The patient passed away in a few hours. DISCUSSION: Chronic BCS presents with complications of cirrhosis; i.e., ascites and rupture of esophageal varices, like in our patient. On CTA, both the hepatic veins and part of the IVC were occluded. In fact, 31% of BCS patients have outflow occlusion at both these locations. However, in our patient, CTA revealed aneurysms in the celiac artery and distal portions of an SMA branch along with left gastric artery bleeding. Multiple arterial aneurysms have been associated with disorders such as PAN, Behcet's, Ehler-Danlos etc. By comparison, there have not been many reports of multiple idiopathic arterial aneurysms in adults. Several of these possible causes were unable to be worked up for due to the acute presentation, although our patient’s history was not typical for these diseases.

An Uncommon Cause of Ascites: A Combination of Budd Chiari Syndrome and Secondary Bacterial Peritonitis in a Postpartum Patient

Acute Budd Chiari syndrome usually presents with new onset ascites and hepatic dysfunction, at times acute liver failure. Here we present an interesting case of secondary bacterial peritonitis and recurrent Budd Chiari syndrome in a patient with Paroxysmal Nocturnal Hemoglobinuria (PNH) in immediate post partum period. Our patient is 26 year old, diagnosed with Budd Chiari syndrome and PNH, 9 years ago who is post partum after a vaginal delivery. Post partum hemorrhage (PPH) complicated her course requiring Bakri balloon tamponade. Few days post partum she developed abdominal distention, fever, new onset ascites, hepatomegaly, and diffuse abdominal tenderness. There was no purulent vaginal discharge. Lab work showed leukocytosis (5.4 K/CUMM), elevated from her normal baseline of 2-3(secondary to aplastic anemia/PNH). Liver enzymes were normal except ALP of 140 IU/L. Paracentesis revealed bacterial peritonitis with absolute neutrophil count of 3273. She was started on appropriate empiric antibiotics. CT scan showed new onset marked hepatomegaly and moderate ascites. In the setting of PNH (pro-coagulant state), suspicion for a recurrent Budd Chiari syndrome was high. Even though the Doppler ultrasound was negative for hepatic/portal vein thrombosis, CT abdomen with contrast in venous phase revealed heterogeneous hepatic enhancement, predominant left hepatic lobe enlargement and non visualization of the hepatic veins; consistent with Budd Chiari Syndrome. We ruled out chronic Budd Chiari Syndrome, although we acknowledge that this can't be done with 100% certainty (Magnetic Resonance angiogram in 2011 did not reveal any features of Budd Chiari syndrome, nor did the periodic obstetric ultrasounds reveal any ascites prepartum). In patients with new onset ascites and hepatomegaly, Budd Chiari syndrome is an important differential in setting of PNH. This patient was at risk for post partum endometritis (in setting of balloon tamponade) which could lead to bacterial peritonitis due to micro-perforations. Considering the purulent ascites with absolute neutrophil count of 3273, we believe a combination of the above two pathologies resulted in this clinical presentation. For Budd Chiari syndrome, duplex imaging studies may not be conclusive, and in cases with high suspicion CT done in venous phase maybe helpful. The ascitic fluid cultures may remain negative as in our case, requiring empiric antibiotic coverage.

Prognostic scoring systems and outcome of endovascular radiological intervention of chronic Budd-Chiari syndrome in children.

Prognostic scoring systems (PSS) have not been validated in children with chronic Budd-Chiari syndrome (BCS). We aimed to analyse the long-term outcome of radiological intervention (RI) and validate the PSS in children. Chronic BCS children were analysed in four subgroups: (i) SI: successful intervention (primary or secondary stent patency) (ii) PO: poor outcome (refractory stent block or requirement of liver transplantation), (iii) NU: naïve unintervened (awaiting RI) and (iv) DBI: died before intervention. PSS analysed included Paediatric end-stage liver disease (PELD), Rotterdam, BCS-Transjuglar intrahepatic Portosystemic shunt (BCS-TIPS) index, Zeitoun, Child-Pugh and Model for end-stage liver disease. Of 113 BCS children, 48 children underwent 53 successful primary RI. Actuarial probability of vascular patency was 87% at 1year and 82% at 5years follow-up. Four groups (SI: n=40, PO: n=7, NU: n=13, DBI: n=6) were analysed. Univariate analysis showed pre-intervention PELD score [PO: 11 (-1-23) vs SI: 2 (-8-25), P=.009] with a cut-off of 4 (AUC: 0.809, 86% sensitivity, 75% specificity) determined PO following intervention. In unintervened group (NU vs DBI), multivariate analysis demonstrated that Zeitoun score predicted death independently (OR 15.4, 95% CI: 1.17-203.56, P=.04) with a cut-off of 4.3 (AUC: 0.923, 83% sensitivity and 77% specificity). Children with BCS have a favourable long-term outcome. Among those undergoing RI, pre-intervention PELD score determines the outcome. Survival is determined by Zeitoun score in those unintervened.

Magnetic Resonance Venography Findings of Obstructed Hepatic Veins and the Inferior Vena Cava in Patients with Budd-Chiari Syndrome

ObjectiveThis study aimed to illustrate the magnetic resonance venography (MRV) manifestations of obstructed hepatic veins (HVs), the inferior vena cava (IVC), and accessory hepatic veins (AHVs) in patients with Budd-Chiari syndrome (BCS) and to evaluate the visualization capacity of MRV in the diagnosis of BCS.Materials and MethodsFifty-two patients with chronic BCS were included in this study. All patients were examined via MRV performed with a 3T system following injections of gadolinium-diethylene triamine pentaacetic acid (Gd-DTPA) or Gd-ethoxibenzyl-DTPA. HV and IVC lesions were classified, and their characteristics were described. HV cord-like occlusions detected via MRV were compared using ultrasonography (US). Digital subtraction angiography (DSA) was performed as a contrast in the MRV detection of IVC lesions. The HVs draining collaterals, mainly AHVs, were carefully observed. HV lesions were classified as segmental stenosis, segmental occlusion, membranous stenosis, membranous occlusion, cord-like occlusion, or non-visualized. Except for patent IVCs, IVC lesions were classified as segmental occlusion, segmental stenosis, membranous occlusion, membranous stenosis, and hepatomegaly-induced stenosis.ResultsAll patients (52/52, 100%) showed HV lesions of different degrees. MRV was inferior to US in detecting cord-like occlusions (6 vs. 19, χ2 = 11.077, p < 0.001). Dilated AHVs, including 50 (50/52, 96.2%) caudate lobe veins and 37 (37/52, 71.2%) inferior HV and AHV lesions, were well-detected. There were no significant differences in detecting segmental lesions and thrombosis between MRV and DSA (χ2 = 0.000, p1 = 1.000, p2 = 1.000). The capacity of MRV to detect membranous lesions was inferior to that of DSA (7 vs. 15, χ2 = 6.125, p = 0.013).ConclusionIn patients with BCS, MRV can clearly display the lesions in HVs and the IVC, as well as in AHVs, and it has diagnostic and therapeutic value.